The effect of melatonin and epiphysectomy on the function of the mono-oxygenase system in rat liver

After chronic melatonin administration (1 mg/kg, 14 days) the content of cytochrome P-450 and activity of NADPH: cytochrome c-reductase in rat microsomes were increased. Pinealectomized rats had opposite directed shifts in microsomal oxidation. In these animals activated effect of melatonin was absent.     

Transformation of the ground cover after surface fires and estimation of pyrogenic carbon emissions in the dark-coniferous forests of Central Siberia

Ground fuel loads and structure in dark-coniferous forests with the dominance of Siberian pine have been studied in the Central Siberian State Nature Biosphere Reserve located in the central-taiga zone of Central Siberia. The impacts of surface fires of various forms and severity on the living ground cover are examined. It is found that fires of low to moderate severity reduce ground fuel loads from 35–49 t/ha to 26–28 t/ha, while fires of moderate to high severity reduce them to 17–18 t/ha. Consumption of down woody debris varies from 3 to 29 t/ha, depending on the prefire fuel characteristics and fire form and severity. Steady fires spreading with the fire danger index PV-1 of 3919 ± 482 result in carbon emissions of 14.0 tC/ha from fires of low to moderate severity and 24.6 tC/ha from fires of moderate to high severity. The lowest carbon emissions (10.1 tC/ha) are noted for fast-moving fires spreading with PV-1 of 1167 ± 386.     

Theoretical Study of Antagonists and Inhibitors of Mammalian Adenosine Deaminase: II. Isomeric Aza-deazaanalogues of Adenosine

Isomeric aza-deazaanalogues of adenosine and their N1-protonated forms (except for that of 8-aza-1-deazaadenosine) were studied by computer modeling to find a relationship between their molecular structures and the properties as substrates for the mammalian adenosine deaminase. The atomic charge distribution and maps of electrostatic potential around their van der Waals molecular surface were calculated using the ab initioSTO-3G method. The conformational studies were carried out by the MM⁺ method of molecular mechanics. The previously proposed mechanism of the substrate acceptance in the active site of mammalian adenosine deaminase was refined, and the potential substrate properties were predicted for two previously unstudied adenosine analogues, 5-aza-9-deazaadenosine and 8-aza-3-deazaadenosine.     

Theoretical study of antagonists and inhibitors of mammalian adenosine deaminase. I. Adenosine and its aza- and deaza-analogs

Aza- and deazaanalogues of adenosine, including their 1-protonated forms (except for that of 1-deazaadenosine), were studied by computer computation to find a relationship between their molecular structures and substrate properties for the mammalian adenosine deaminase. The atomic charge distribution and maps of the electrostatic potential around their van der Waals molecular surface were calculated for these compounds using the ab initio STO-3G method. The conformational studies were carried out by the MM+ method of molecular mechanics. The mechanism that determines the substrate selectivity of mammalian adenosine deaminase is discussed. The English version of the paper: Russian Journal of Bioorganic Chemistry, 2002, vol. 28, no. 4; see also http://www.maik.ru.     

Theoretical Study of the Structure of Adenosine Deaminase Complexes with Adenosine Analogues: I. Aza-, Deaza-, and Isomeric Azadeazaanalogues of Adenosine

Conformational models of the active site of adenosine deaminase (ADA) and its complexes in the basic state with adenosine and 13-isosteric analogues of the aza, deaza, and azadeaza series were constructed. The optimization of the conformational energy of the active site and the nucleoside bound with it in the complex was achieved in the force field of the whole enzyme [the structure of ADA complex with 1-deazaadenosine (1ADD) was used] within the molecular mechanics model using the AMBER 99 potentials. The stable conformational states of each of the complexes, as well as the optimal conformation of ADA in the absence of ligand, were determined. It was proved that the conformational state that is close to the structure of the ADA complex with 1ADD known from X-ray study corresponds to one of the local minima of the potential surface. Another, a significantly deeper minimum was determined; it differs from the first minimum by the mutual orientation of side chains of amino acid residues. A similar conformational state is optimal for the ADA active site in the absence of bound ligand. A qualitative correlation exists between the values of potential energies of the complexes in this conformation and the enzymatic activity of ADA toward the corresponding nucleosides. The dynamics of conformational conversions of the active site after the binding of substrate or its analogues, as well as the possibility of the estimation of the inhibitory properties of nucleosides on the basis of calculations, are discussed.     

Distinct roles of basal steady-state and induced H-ferritin in tumor necrosis factor-induced death in L929 cells

Tumor necrosis factor (TNF) alpha is a cytokine capable of inducing caspase-dependent (apoptotic) cell death in some cells and caspase-independent (necrosis-like) cell death in others. Here, using a mutagenesis screen for genes critical in TNF-induced death in L929 cells, we have found that H-ferritin deficiency is responsible for TNF resistance in a mutant line and that, upon treatment with TNF, this line fails to elevate levels of labile iron pool (LIP), critical for TNF-induced reactive oxygen species (ROS) production and ROS-dependent cell death. Since we found that TNF-induced LIP in L929 cells is primarily furnished by intracellular storage iron, the lesser induction of LIP in H-ferritin-deficient cells results from a reduction of intracellular iron storage caused by less H-ferritin. Different from some other cell lines, the H-ferritin gene in L929 cells is not TNF inducible; however, when H-ferritin is expressed in L929 cells under a TNF-inducible system, the TNF-induced LIP and subsequent ROS production and cell death were all prevented. Thus, LIP is a common denominator of ferritin both in the enhancement of cell death by basal steady-state H-ferritin and in protection against cell death by induced H-ferritin, thereby acting as a key determinant of TNF-induced cell death.     

MicroRNAs as the Potential Regulators of SARS-CoV-2 Infection and Modifiers of the COVID-19 Clinical Features

Molecular Biology - The pandemic of coronavirus disease 2019 (COVID-19) warrants the identification of factors that may determine both risk and severity of infection. The factors include microRNAs...     

Protocol of Transcriptome Analysis of Decidual Placenta Cells

Molecular Biology - The advent of high-throughput sequencing technologies has expanded our understanding of the biological significance of non-coding regions of the genome. In recent years, more...